Recently, the present inventors have shown that isoniazid specifically substituted in the acyl position with 13C greatly increase isoniazid activity, through enhanced formation of INH-NAD and NADP adducts after its activation by the bacterial enzyme KatG, with these adducts being the species that are highly toxic to mycobacteria. It is believed that this is due to kinetic isotope effects on several steps of the pathway, although effects in the reversibility of acyl radical addition to the NAD, perhaps play the major role. It has been shown that another major TB drug, ethionamide (and its related compound prothionamide), undergoes almost identical activation and adduct formation chemistries (Wang, et al J Exp Med 204 73-8 2007). This chemistry is shown in FIG. 1 attached, with a highly reversible initial adduct being formed.